Up-Regulation of Akt and Nav1.8 in BmK I-Induced Pain
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As the key contributor to the rising phase of action potentials in dorsal root ganglion (DRG) neurons, voltage-gated sodium channels (VGSCs) are important in physiological and pathological pain conditions. For instance, abnormal expression of VGSCs in DRG neurons is the main cause of the induction and maintenance of chronic inflammatory pain. Previously, we have reported that functional up-regulation of a peripheral VGSC isoform Nav1.8 is critical in pain behaviors induced by BmK I, a sodium channel activator purified from the venom of Buthus martensi Karsch (BmK) . It is well known that protein kinase B/Akt participates in multiple cellular processes including protein synthesis, cell survival, proliferation, and metabolism. Moreover, it has been demonstrated that the Akt pathway plays an indispensable role in the hyperexcitability of peripheral sensory neurons and therefore contributes to the generation and maintenance of pathological pain [2, 3]. The activation of...
This work was supported by grants from the National Natural Science Foundation of China (31571032, 31771191, and 81402903). ZYT was supported by an Indiana Spinal Cord and Brain Injury Research Fund grant (ISCBIRF2017) from the Indiana State Department of Health.
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Conflict of interest
The authors declare that there are no competing interest.